New Zealand (NZB and NZB/W) mice develop genetically determined autoimmune and immunoproliferative syndromes that resemble systemic lupus erythematosus (SLE) and a spectrum of lymphoproliferative disorders of human beings. Our studies have shown that the multifactorial pathogenesis of the SLE-like nephritis of these mice is related not only to nucleoprotein antigen-antibody complexes but also to the circulation and deposition of the 70,000 mol. wt. viral envelope glycoprotein, gp70, encoded by the endogenous type C RNA virus (retrovirus). We next turned to a search for possible evidence of type C viral antigen expression in human tissues obtained in a variety of conditions and diseases, including SLE. The laboratory confirmed the electron microscopic findings of rare to frequent atypical type C virus-like particles in the term placental trophoblastic tissues of normal patients, as described by others, and of SLE patients as well. We next found that a putative retroviral antigen was present in focal deposits in the renal glomerular lesions of SLE patients who had lupus proliferative glomerulonephritis and was not detectable in any other human condition studied. We then extended this finding by eluting, and characterizing, a retrovirus-reactive human antibody recovered from the same lesions. We have developed sensitive and specific enzymoimmunoassays for the detection and measurement of the major structural (p30) protein of primate type C viruses and are applying these assays to the analysis of purified extracts of human normal and pathological tissues.